Microelectrode arrays used to record local field potentials from the brain are being built with increasingly more spatial resolution, ranging from the initially developed laminar arrays to those with planar and three-dimensional (3D) formats. In parallel with such development in recording techniques, current source density (CSD) analyses have recently been expanded up to the continuous-3D form. Unfortunately, the effect of the conductivity profile on the CSD analysis performed with contemporary microelectrode arrays has not yet been evaluated and most of the studies assumed it was homogeneous and isotropic. In this study, we measured the conductivity profile in the somatosensory barrel cortex of Wistar rats. To that end, we combined multisite electrophysiological data recorded with a homemade assembly of silicon-based probes and a nonlinear least-squares algorithm that implicitly assumed that the cerebral cortex of rodents could be locally approximated as a layered anisotropic spherical volume conductor. The eccentricity of the six cortical layers in the somatosensory barrel cortex was evaluated from postmortem histological images. We provided evidence for the local spherical character of the entire barrels field, with concentric cortical layers. We found significant laminar dependencies in the conductivity values with radial/tangential anisotropies. These results were in agreement with the layer-dependent orientations of myelinated axons, but hardly related to densities of cells. Finally, we demonstrated through simulations that ignoring the real conductivity profile in the somatosensory barrel cortex of rats caused considerable errors in the CSD reconstruction, with pronounced effects on the continuous-3D form and charge-unbalanced CSD. We concluded that the conductivity profile must be included in future developments of CSD analysis, especially for rodents.

These results suggest that the peripheral AI(r) measurement is clinically useful in predicting LVH. Enhanced wave reflection may be related to the development of LVH in hypertensive patients.

The quantification of spontaneous calcium (Ca(2+)) oscillations (SCOs) in astrocytes presents a challenge because of the large irregularities in the amplitudes, durations, and initiation times of the underlying events. In this article, we use a stochastic context to account for such SCO variability, which is based on previous models for cellular Ca(2+) signaling. First, we found that passive Ca(2+) influx from the extracellular space determine the basal concentration of this ion in the cytosol. Second, we demonstrated the feasibility of estimating both the inositol 1,4,5-trisphosphate (IP(3)) production levels and the average number of IP(3) receptor channels in the somatic clusters from epifluorescent Ca(2+) imaging through the combination of a filtering strategy and a maximum-likelihood criterion. We estimated these two biophysical parameters using data from wild-type adult mice and age-matched transgenic mice overexpressing the 695-amino-acid isoform of human Alzheimer β-amyloid precursor protein. We found that, together with an increase in the passive Ca(2+) influx, a significant reduction in the sensitivity of G protein-coupled receptors might lie beneath the abnormalities in the astrocytic Ca(2+) signaling, as was observed in rodent models of Alzheimer's disease. This study provides new, to our knowledge, indices for a quantitative analysis of SCOs in normal and pathological astrocytes.

Spontaneous calcium (Ca2+) oscillations (SCOs) in astrocytes might be a crucial signaling for the multipurpose role of this type of cell in several brain functions. To interpret experimental data of astrocytic SCOs, which has been largely observed in the last decade, several groups have attempted to accommodate biophysical models that were developed in the past for Ca2+ signaling in other cell types. In most of the cases, only predictive strategies were used to estimate specific parameters of these modified models from actual experiments. In this study, we discuss the most remarkable models used to describe Ca2+ signaling in astrocytes. At the same time, we aim to revise the particulars of applying these models to interpret epifluorescent time series obtained from large regions of interest. Specially, we developed a detailed model for global Ca2+ signaling in the somata of astrocytes. In order to estimate some of the parameters in our model, we propose a deductive reasoning strategy, i.e., a statistical inference method that results from combining a filtering technique and a maximum likelihood principle. By means of computer simulations, we evaluate the accuracy of this estimation's strategy. Finally, we use the new model, in combination with a recent experimental findings by our group, to estimate the degree of cluster coupling inside the soma during the genesis of global Ca2+ events.

Background: Arterial stiffness is a risk factor for symptomatic stroke, and is associated with symptomatic cerebral infarction and cognitive impairment. Hence, we hypothesized that arterial stiffness would be a significant determinant of silent cerebrovascular lesions. Methods: The subjects were 363 individuals without symptomatic cerebrovascular lesions who had their arterial stiffness assessed by brachial-ankle pulse wave velocity (baPWV) measurement. The subjects were classified into two groups by the presence or absence of lacunar infarcts, as well as into three groups by grade of white matter hyperintensity (WMH). baPWV was compared among these groups. Results: Eighty-six subjects had lacunar infarcts. Of 138 subjects with WMHs, 102 were classified as having grade 1 and 36 as having grade 2 or 3 WMHs. baPWV was significantly higher in subjects with lacunar infarcts than in those without (17.3 ± 0.3 vs. 16.4 ± 0.2 m/s). baPWV tended to increase with higher WMH grade (16.2 ± 0.2, 16.9 ± 0.3, and 17.8 ± 0.5 m/s in grade 0, 1, and 2 or 3, respectively) after adjustments for confounding factors. The adjusted odds ratio (OR) for lacunar infarcts in subjects with middle-tertile baPWV was significantly higher (OR, 2.37; 95% confidence interval, CI, 1.10–5.11) and the OR in subjects with the highest-tertile baPWV tended to be higher (OR 2.26; 95% CI 0.99–5.45) compared with the lowest-tertile baPWV. The adjusted OR for WMH tended to increase with increased baPWV. Conclusions: Arterial stiffness appeared to be associated with the presence of a lacunar infarct and WMH, independently of the risks for other cerebrovascular diseases.